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Obesity: HELP
Articles by Y. Liu
Based on 24 articles published since 2010
(Why 24 articles?)
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Between 2010 and 2020, Y. Liu wrote the following 24 articles about Obesity.
 
+ Citations + Abstracts
1 Review Gut microbiota and obesity-associated osteoarthritis. 2019

Liu, Y / Ding, W / Wang, H L / Dai, L L / Zong, W H / Wang, Y Z / Bi, J / Han, W / Dong, G J. ·School of Kinesiology, Shanghai University of Sport, Shanghai, China; Shandong Sport University, Jinan, China. · Department of Construction and Real Estate Management, Laiyang, China; Shandong Sport University, Jinan, China. · College of Physical Education, Henan Normal University, Xinxiang, China. · Shandong Sport University, Jinan, China. · School of Kinesiology, Shanghai University of Sport, Shanghai, China; Shandong Sport University, Jinan, China. Electronic address: donggj@163.com. ·Osteoarthritis Cartilage · Pubmed #31146016.

ABSTRACT: Obesity is a well-known primary risk factor for osteoarthritis (OA). In recent decades, the biomechanics-based theoretical paradigm for the pathogenesis of obesity-associated OA has been gradually but fundamentally modified. This modification is a result of accumulating evidence that biological factors also contribute to the etiology of the disease. The gut microbiota is a complicated ecosystem that profoundly influences the health of the host and can be modulated by the combined effects of environmental stimuli and genetic factors. Recently, enteric dysbacteriosis has been identified as a causal factor in the initiation and propagation of obesity-associated OA in animal models. Gut microbes and their components, microbe-associated lipid metabolites, and OA interact at both systemic and local levels through mechanisms that involve interplay with the innate immune system. However, the demonstration of causality in humans will require further studies. Nonetheless, probiotics, prebiotics, dietary habits and exercise, which aid the restoration of a healthy microbial community, are potential therapeutic approaches in the treatment of obesity-associated OA.

2 Review [Effect of liraglutide in treatment of non-alcoholic fatty liver disease: mechanism of action and research advances]. 2017

Liu, Y / Feng, P P / Zhu, W / Gong, J P. ·Department of Gastroenterology, The fifth people's Hospital of Chengdu, Chengdu 611130, China. · Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China. ·Zhonghua Gan Zang Bing Za Zhi · Pubmed #28763870.

ABSTRACT: Non-alcoholic fatty liver disease is a common chronic liver disease closely associated with obesity, hyperlipidemia, and diabetes. It can gradually progress to liver cirrhosis or even hepatocellular carcinoma; however, there are still no specific therapeutic agents for this disease. Liraglutide is a human glucagon-like peptide-1 analogue and has a marked effect in the treatment of type 2 diabetes. At present, many studies indicate that liraglutide also has a certain therapeutic effect on non-alcoholic fatty liver disease during the treatment of type 2 diabetes, but its mechanism of action remains unknown. This article reviews the known mechanisms of action of liraglutide in the treatment of non-alcoholic fatty liver disease.

3 Article Associations between Sarcopenic Obesity and Cognitive Impairment in Elderly Chinese Community-Dwelling Individuals. 2019

Wang, H / Hai, S / Liu, Y X / Cao, L / Liu, Y / Liu, P / Yang, Y / Dong, B R. ·Birong Dong, Center of Gerontology and Geriatrics, West China Hospital, Sichuan University, No. 37 Guoxue Lane, Chengdu 610041, China, E-mail address: birongdong@163.com. ·J Nutr Health Aging · Pubmed #30569063.

ABSTRACT: INTRODUCTION: This study aimed to estimate the prevalence of sarcopenic obesity (SO) and the association between cognitive impairment and SO in a cohort of elderly Chinese community-dwelling individuals. METHODS: A total of 948 elderly Chinese community-dwelling individuals aged 60-92 years were recruited. The participants were categorized into the following four groups according to their sarcopenia and obesity status: sarcopenic obese, sarcopenic, obese and non-sarcopenic, and non-obese group. Sarcopenia was defined as appendicular skeletal muscle index of <7.0 kg/m2 in men and <5.7 kg/m2 in women; obesity was defined as values greater than the upper two quintiles for body fat percentage stratified by gender of the study population; cognitive impairment was measured using the Mini-Mental State Examination and defined as a score of <24. RESULTS: A total of 945 participants were included in the statistical analyses with a mean age of 68.76 ± 6.50 years. The prevalence of SO was 6.0% (7.3% in men and 4.8% in women). The sarcopenic obese (odds ratio [OR]: 2.550, 95% confidence interval [CI], 1.196-5.435) and obese (ORs: 2.141, 95% CI, 1.230-3.728) groups had significantly increased risk for cognitive impairment in fully adjusted model, respectively. CONCLUSION: The SO prevalence in elderly Chinese community-dwelling individuals was relatively low (6.0%). The present study suggested SO was independently associated with cognitive impairment.

4 Article [Relations between pregestational body mass index, gestational weight gain and birth weight of neonates among women in the Southwest areas of China: A prospective cohort study]. 2018

Li, D T / Liang, Y / Gong, Y H / Chen, M X / Feng, P / Yang, D G / Yang, W Y / Liu, Y / Cheng, G. ·Department of Nutrition, Food Safety and Toxicology, West China School of Public Health. · Department of Obstetrics and Gynecology, West China Second University Hospital. · Sichuan University, Chengdu 610041, China; Department of Clinical Nutrition, Affiliated Hospital of Guizhou Medical University, Guiyang 550001, China. ·Zhonghua Liu Xing Bing Xue Za Zhi · Pubmed #30453430.

ABSTRACT:

5 Article A J-shaped relation of BMI and stroke: Systematic review and dose-response meta-analysis of 4.43 million participants. 2018

Liu, X / Zhang, D / Liu, Y / Sun, X / Hou, Y / Wang, B / Ren, Y / Zhao, Y / Han, C / Cheng, C / Liu, F / Shi, Y / Chen, X / Liu, L / Chen, G / Hong, S / Zhang, M / Hu, D. ·The Affiliated Luohu Hospital of Shenzhen University Health Sciences Center, Shenzhen, Guangdong, People's Republic of China; Department of Preventive Medicine, Shenzhen University Health Sciences Center, Shenzhen, Guangdong, People's Republic of China. · The Affiliated Luohu Hospital of Shenzhen University Health Sciences Center, Shenzhen, Guangdong, People's Republic of China. · College of Physical Education, Zhengzhou University, Zhengzhou, Henan, People's Republic of China. · The Affiliated Luohu Hospital of Shenzhen University Health Sciences Center, Shenzhen, Guangdong, People's Republic of China; Department of Preventive Medicine, Shenzhen University Health Sciences Center, Shenzhen, Guangdong, People's Republic of China; Department of Epidemiology and Health Statistics, College of Public Health, Zhengzhou University, Zhengzhou, Henan, People's Republic of China. · Department of Epidemiology and Health Statistics, College of Public Health, Zhengzhou University, Zhengzhou, Henan, People's Republic of China. · Department of Preventive Medicine, Shenzhen University Health Sciences Center, Shenzhen, Guangdong, People's Republic of China. · Department of Clinical Medicine, Shenzhen University Health Sciences Center, Shenzhen, Guangdong, People's Republic of China. · The Affiliated Luohu Hospital of Shenzhen University Health Sciences Center, Shenzhen, Guangdong, People's Republic of China; Department of Preventive Medicine, Shenzhen University Health Sciences Center, Shenzhen, Guangdong, People's Republic of China. Electronic address: hud@szu.edu.cn. ·Nutr Metab Cardiovasc Dis · Pubmed #30287124.

ABSTRACT: BACKGROUND AND AIM: Many studies have shown increased risk of stroke with greater adiposity as measured by body mass index (BMI), but questions remain about the shape of the dose-response relation. We conducted a systematic review and meta-analysis of prospective studies to clarify the strength and shape of the dose-response relation between BMI and risk of stroke. METHODS AND RESULTS: PubMed and Embase databases were searched for articles published up to May 11, 2018. Random-effects generalized least-squares regression models were used to estimate study-specific dose-response association, and restricted cubic splines were used to model the association. We included reports of 44 prospective cohort studies describing 102 466 incident cases among 4 432 475 participants. With a 5-unit increment in BMI, the summary relative risk for stroke incidence was 1.10 (95% confidence interval, 1.06 to 1.13; I CONCLUSION: Both overweight and obesity increase the risk of stroke with a J-shaped dose-response relation, and the nadir of the curve was observed at BMI 23-24 kg/m

6 Article [The role of cytochrome P450 in nonalcoholic fatty liver induced by high-fat diet: a gene expression profile analysis]. 2017

Liu, Y / Cheng, F / Luo, Y X / Hu, P / Ren, H / Peng, M L. ·Key Laboratory of Molecular Biology for Infectious Diseases, Institute for Viral Hepatitis, Department of Infectious Diseases, Chinese Ministry of Education, the Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China. ·Zhonghua Gan Zang Bing Za Zhi · Pubmed #28494548.

ABSTRACT:

7 Article Molecular Profiling of Human Induced Pluripotent Stem Cell-Derived Hypothalamic Neurones Provides Developmental Insights into Genetic Loci for Body Weight Regulation. 2017

Yao, L / Liu, Y / Qiu, Z / Kumar, S / Curran, J E / Blangero, J / Chen, Y / Lehman, D M. ·Department of Cell Systems and Anatomy, University of Texas Health Science Center, San Antonio, TX, USA. · Department of Microbiology and Immunology, University of Texas Health Science Center, San Antonio, TX, USA. · South Texas Diabetes and Obesity Institute (STDOI), University of Texas Rio Grande Valley (UTRGV) School of Medicine, Brownsville, TX, USA. · Department of Epidemiology and Biostatistics, Greehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, TX, USA. · Department of Medicine, University of Texas Health Science Center, San Antonio, TX, USA. ·J Neuroendocrinol · Pubmed #28071834.

ABSTRACT: Recent data suggest that common genetic risks for metabolic disorders such as obesity may be human-specific and exert effects via the central nervous system. To overcome the limitation of human tissue access for study, we have generated induced human pluripotent stem cell (hiPSC)-derived neuronal cultures that recapture many features of hypothalamic neurones within the arcuate nucleus. In the present study, we have comprehensively characterised this model across development, benchmarked these neurones to in vivo events, and demonstrate a link between obesity risk variants and hypothalamic development. The dynamic transcriptome across neuronal maturation was examined using microarray and RNA sequencing methods at nine time points. K-means clustering of the longitudinal data was conducted to identify co-regulation and microRNA control of biological processes. The transcriptomes were compared with those of 103 samples from 13 brain regions reported in the Genotype-Tissue Expression database (GTEx) using principal components analysis. Genes with proximity to body mass index (BMI)-associated genetic variants were mapped to the developmentally expressed genesets, and enrichment significance was assessed with Fisher's exact test. The human neuronal cultures have a transcriptional and physiological profile of neuropeptide Y/agouti-related peptide arcuate nucleus neurones. The neuronal transcriptomes were highly correlated with adult hypothalamus compared to any other brain region from the GTEx. Also, approximately 25% of the transcripts showed substantial changes in expression across neuronal development and potential co-regulation of biological processes that mirror neuronal development in vivo. These developmentally expressed genes were significantly enriched for genes in proximity to BMI-associated variants. We confirmed the utility of this in vitro human model for studying the development of key hypothalamic neurones involved in energy balance and show that genes at loci associated with body weight regulation may share a pattern of developmental regulation. These data support the need to investigate early development to elucidate the human-specific central nervous system pathophysiology underlying obesity susceptibility.

8 Article Role of vitamin A metabolism in IIH: Results from the idiopathic intracranial hypertension treatment trial. 2017

Libien, J / Kupersmith, M J / Blaner, W / McDermott, M P / Gao, S / Liu, Y / Corbett, J / Wall, M / Anonymous4200891. ·Pathology, State University of New York, Downstate School of Medicine, Brooklyn, NY, United States. · Neurology and Ophthalmology, Mount Sinai West, Icahn School of Medicine at Mount Sinai, New York, NY, United States. Electronic address: mkuper@chpnet.org. · Medicine, College of Physicians and Surgeons, Columbia University School of Medicine, New York, NY, United States. · Biostatistics, University of Rochester, Rochester, NY, United States. · Neurology, University of Mississippi School of Medicine, Jackson, MS, United States. · Neurology, University of Iowa School of Medicine, Iowa City, IA, United States. ·J Neurol Sci · Pubmed #28017254.

ABSTRACT: INTRODUCTION: Vitamin A and its metabolites (called retinoids) have been thought to play a role in the development of idiopathic intracranial hypertension (IIH). The IIH Treatment Trial (IIHTT) showed the efficacy of acetazolamide (ACZ) in improving visual field function, papilledema grade, quality of life and cerebrospinal fluid (CSF) pressure. We postulated that IIH patients would demonstrate elevated measures of vitamin A metabolites in the serum and CSF. METHODS: Comprehensive measures of serum vitamin A and its metabolites were obtained from 96 IIHTT subjects, randomly assigned to treatment with ACZ or placebo, and 25 controls with similar gender, age and body mass index (BMI). These included retinol, retinol binding protein, all-trans retinoic acid (ATRA), alpha- and beta-carotenes, and beta-cryptoxanthin. The IIHTT subjects also had CSF and serum vitamin A and metabolite measurements obtained at study entry and at six months. RESULTS: At study entry, of the vitamin A metabolites only serum ATRA was significantly different in IIHTT subjects (median 4.33nM) and controls (median 5.04nM, p=0.02). The BMI of IIHTT subjects showed mild significant negative correlations with serum ATRA, alpha- and beta-carotene, and beta-cryptoxanthin. In contrast, the control subject BMI correlated only with serum ATRA. At six months, the serum retinol, alpha-carotene, beta-carotene, and CSF retinol were increased from baseline in the ACZ treated group, but only increases in alpha-carotene (p=0.02) and CSF ATRA (p=0.04) were significantly greater in the ACZ group compared with the placebo group. No other vitamin A measures were significantly altered over the six months in either treatment group. Weight loss correlated with only with the change in serum beta-carotene (r=-0.44, p=0.006) and the change in CSF retinol (r=-0.61, p=0.02). CONCLUSION: Vitamin A toxicity is unlikely a contributory factor in the causation of IIH. Our findings differ from those of prior reports in part because of our use of more accurate quantitative methods and measuring vitamin A metabolites in both serum and CSF. ACZ may alter retinoid metabolism in IIH patients.

9 Article The role and possible mechanism of lncRNA U90926 in modulating 3T3-L1 preadipocyte differentiation. 2017

Chen, J / Liu, Y / Lu, S / Yin, L / Zong, C / Cui, S / Qin, D / Yang, Y / Guan, Q / Li, X / Wang, X. ·Department of Cell Biology, Shandong University School of Medicine, Jinan, Shandong, China. · Department of Endocrinology, Qingdao Municipal Hospital, Qingdao, Shandong, China. · Department of Laboratory Medicine, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, Shandong, China. · Department of Endocrinology, Shandong Provincial Hospital, Affiliated to Shandong University, Jinan, Shandong, China. · Key Laboratory of Protein Sciences for Chronic Degenerative Diseases, Universities of Shandong (Shandong University), Jinan, Shandong, China. ·Int J Obes (Lond) · Pubmed #27780975.

ABSTRACT: BACKGROUND: Obesity is a risk factor for metabolic diseases, while preadipocyte differentiation or adipogenesis is closely related to obesity occurrence. Long noncoding RNAs (lncRNAs) are a unique class of transcripts in regulation of a variety of biological processes. Using cDNA microarray, we found lncRNA U90926 is negatively correlated with 3T3-L1 preadipocyte differentiation. OBJECTIVE: The aim of this study was to explore the role of lncRNA U90926 (lnc-U90926) in adipogenesis and the underlying mechanisms. METHODS: Quantitative real-time PCR (qPCR) was performed to determine lnc-U90926 expression in 3T3-L1 preadipocytes, differentiated adipocytes, and in adipose tissues form mice. RNA fluorescent in situ hybridization (FISH) was performed to determine the localization of lnc-U90926 in 3T3-L1 preadipocytes. The effects of lnc-U90926 on 3T3-L1 adipogenesis were analyzed with lentivirus-mediated gain- and loss-of-function experiments. Lipid accumulation was evaluated by oil red O staining; several adipogenesis makers were analyzed by qPCR and western blotting. Dual luciferase assay was applied to explore the transactivation of target genes modulated by lnc-U90926. All measurements were performed at least for three times. RESULTS: Lnc-U90926 expression decreased along the differentiation of 3T3-L1 preadipocytes. In mice, lnc-U90926 is predominantly expressed in adipose tissue. Obese mice have lower lnc-U90926 expression in subcutaneous and visceral adipose tissue than non-obese mice. FISH results showed that lnc-U90926 was mainly located in the cytoplasm. Overexpression lnc-U90926 attenuated 3T3-L1 adipocyte differentiation as evidenced by its ability to inhibit lipid accumulation, to decrease the mRNA levels of peroxisome proliferator-activated receptor gamma 2 (PPARγ2), fatty acid binding protein 4 (FABP4) and adiponectin (AdipoQ) as well as to reduce the protein levels of PPARγ and FABP4 (P<0.05). Knockdown of lnc-U90926 showed opposite effects, which increased mRNA expression of PPARγ2, FABP4, CCAAT/enhancer-binding proteinα (C/EBPα) and AdipoQ. CONCLUSION: Lnc-U90926 attenuates 3T3-L1 adipocyte differentiation via inhibiting the transactivation of PPARγ2 or PPARγ.

10 Article High fat induces acute and chronic inflammation in the hypothalamus: effect of high-fat diet, palmitate and TNF-α on appetite-regulating NPY neurons. 2017

Dalvi, P S / Chalmers, J A / Luo, V / Han, D-Yd / Wellhauser, L / Liu, Y / Tran, D Q / Castel, J / Luquet, S / Wheeler, M B / Belsham, D D. ·Department of Physiology, University of Toronto, Toronto, Ontario, Canada. · Unité de Biologie Fonctionnelle et Adaptative, University of Paris Diderot, Sorbonne Paris Cité, CNRS UMR 8251, Paris, France. · Department of Medicine, University of Toronto, Toronto, Ontario, Canada. · Division of Cellular and Molecular Biology, Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, Canada. · Department of Obstetrics and Gynecology, University of Toronto, Toronto, Ontario, Canada. ·Int J Obes (Lond) · Pubmed #27773938.

ABSTRACT: BACKGROUND: Consumption of dietary fat is one of the key factors leading to obesity. High-fat diet (HFD)-induced obesity is characterized by induction of inflammation in the hypothalamus; however, the temporal regulation of proinflammatory markers and their impact on hypothalamic appetite-regulating neuropeptide Y/agouti-related peptide (NPY/AgRP) neurons remains undefined. METHODS: Mice were injected with an acute lipid infusion for 24 h or fed a HFD over 8-20 weeks. Characterized mouse NPY/AgRP hypothalamic cell lines were used for in vitro experimentation. Immunohistochemistry in brain slices or quantitative real-time PCR in cell lines, was performed to determine changes in the expression of key inflammatory markers and neuropeptides. RESULTS: Hypothalamic inflammation, indicated by tumor necrosis factor (TNF)-α expression and astrocytosis in the arcuate nucleus, was evident following acute lipid infusion. HFD for 8 weeks suppressed TNF-α, while significantly increasing heat-shock protein 70 and ciliary neurotrophic factor, both neuroprotective components. HFD for 20 weeks induced TNF-α expression in NPY/AgRP neurons, suggesting a detrimental temporal regulatory mechanism. Using NPY/AgRP hypothalamic cell lines, we found that palmitate provoked a mixed inflammatory response on a panel of inflammatory and endoplasmic reticulum (ER) stress genes, whereas TNF-α significantly upregulated IκBα, nuclear factor (NF)-κB and interleukin-6 mRNA levels. Palmitate and TNF-α exposure predominantly induced NPY mRNA levels. Utilizing an I kappa B kinase β (IKKβ) inhibitor, we demonstrated that these effects potentially occur via the inflammatory IKKβ/NF-κB pathway. CONCLUSIONS: These findings indicate that acute lipid and chronic HFD feeding in vivo, as well as acute palmitate and TNF-α exposure in vitro, induce markers of inflammation or ER stress in the hypothalamic appetite-stimulating NPY/AgRP neurons over time, which may contribute to a dramatic alteration in NPY/AgRP content or expression. Acute and chronic HFD feeding in vivo temporally regulates arcuate TNF-α expression with reactive astrocytosis, which suggests a time-dependent neurotrophic or neurotoxic role of lipids.

11 Article Relevance of omental pericellular adipose tissue collagen in the pathophysiology of human abdominal obesity and related cardiometabolic risk. 2016

Michaud, A / Tordjman, J / Pelletier, M / Liu, Y / Laforest, S / Noël, S / Le Naour, G / Bouchard, C / Clément, K / Tchernof, A. ·Department of Endocrinology and Nephrology, CHU de Quebec-Laval University, Quebec City, Québec, Canada. · School of Nutrition, Laval University, Quebec City, Québec, Canada. · Quebec Heart and Lung Institute, Quebec City, Québec, Canada. · Nutrition Department, Institute of Cardiometabolism and Nutrition, Assistance Publique-Hôpitaux de Paris, Pitié-Salpétrière Hospital, Paris, France. · Sorbonne Universités, UPMC Université Paris 06, Paris, France. · Gynecology Unit, Laval University Medical Center, Ville de Québec, Québec, Canada. · Department of Pathology, Assistance Publique-Hôpitaux de Paris (AP-HP), Pitié-Salpêtrière Hospital, UIMAP, UPMC Université Paris 06, Paris, France. ·Int J Obes (Lond) · Pubmed #27698346.

ABSTRACT: BACKGROUND: Adipose tissue fibrosis is a relatively new notion and its relationship with visceral obesity and cardiometabolic alterations remains unclear, particularly in moderate obesity. OBJECTIVE: Our objective was to examine if total and pericellular collagen accumulation are relevant for the pathophysiology of visceral obesity and related cardiometabolic risk. SUBJECTS AND METHODS: Surgical omental (OM) and subcutaneous (SC) fat samples were obtained in 56 women (age: 47.2±5.8 years; body mass index (BMI): 27.1±4.4 kg/m RESULTS: We found that only pericellular collagen percentage, especially in OM fat, was associated with higher BMI, body fat mass and adipose tissue areas as well as lower radiologic attenuation of visceral adipose tissue and altered cardiometabolic risk variables. Strong correlations between peri-adipocyte collagen percentage and total or M2-macrophage percentages were observed in both depots. Total collagen percentage in either compartment was not related to adiposity, fat distribution or cardiometabolic risk. CONCLUSIONS: As opposed to whole tissue-based assessments of adipose tissue fibrosis, collagen deposition around the adipocyte, especially in the OM fat compartment is related to total and regional adiposity as well as altered cardiometabolic risk profile.

12 Article [Relationship between hypertension and body mass index, waist circumference and waist-hip ratio in middle-aged and elderly residents]. 2016

Xiao, Y Q / Liu, Y / Zheng, S L / Yang, Y / Fan, S / Yang, C / Zhang, J H / Ye, Y L. ·Southwest Medical University, Luzhou 646000, China; Nursing Department, Affiliated Hospital, Southwest Medical University, Luzhou 646000, China. · Epidemiology and Statistics Department, Southwest Medical University, Luzhou 646000, China. · Nursing Department, Affiliated Hospital, Southwest Medical University, Luzhou 646000, China. · Nutrition and Food Hygiene Department, Southwest Medical University, Luzhou 646000, China. ·Zhonghua Liu Xing Bing Xue Za Zhi · Pubmed #27655567.

ABSTRACT:

13 Article Recovery of brain structural abnormalities in morbidly obese patients after bariatric surgery. 2016

Zhang, Y / Ji, G / Xu, M / Cai, W / Zhu, Q / Qian, L / Zhang, Y E / Yuan, K / Liu, J / Li, Q / Cui, G / Wang, H / Zhao, Q / Wu, K / Fan, D / Gold, M S / Tian, J / Tomasi, D / Liu, Y / Nie, Y / Wang, G-J. ·Center for Brain Imaging, School of Life Science and Technology, Xidian University, Xi'an, China. · Department of Psychiatry and McKnight Brain Institute, University of Florida, Gainesville, FL, USA. · Xijing Gastrointestinal Hospital, the Fourth Military Medical University, Xi'an, China. · Department of Biomedical Engineering, Peking University, Beijing, China. · Malcom Randall Veterans Affairs Medical Center, Gainesville, FL, USA. · Department of Radiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, China. · Department of Psychiatry, Xijing Hospital, the Fourth Military Medical University, Xi'an, China. · Institute of Automation, Chinese Academy of Sciences, Beijing, China. · Laboratory of Neuroimaging, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD, USA. ·Int J Obes (Lond) · Pubmed #27200505.

ABSTRACT: BACKGROUND/OBJECTIVES: Obesity-related brain structural abnormalities have been reported extensively, and bariatric surgery (BS) is currently the most effective intervention to produce sustained weight reduction in overtly obese (OB) people. It is unknown whether BS can repair the brain circuitry abnormalities concomitantly with long-term weight loss. SUBJECTS/METHODS: In order to investigate whether BS promotes neuroplastic structural recovery in morbidly OB patients, we quantified fractional anisotropy (FA), mean diffusivity (MD) and gray (GM) and white (WM) matter densities in 15 morbidly OB patients and in 18 normal weight (NW) individuals. OB patients were studied at baseline and also 1 month after laparoscopic sleeve gastrectomy surgery. RESULTS: Two-sample t-test between OB (baseline) and NW groups showed decreased FA values, GM/WM densities and increased MD value in brain regions associated with food intake control (that is, caudate, orbitofrontal cortex, body and genu of corpus callosum) and cognitive-emotion regulation (that is, inferior frontal gyrus, hippocampus, insula, external capsule) (P<0.05, family-wise error correction). Paired t-test in the OB group between before and after surgery showed that BS generated partial neuroplastic structural recovery in the OB group, but the differences had relative less strength and smaller volume (P<0.001). CONCLUSIONS: This study provides the first anatomical evidence for BS-induced acute neuroplastic recovery that might in part mediate the long-term benefit of BS in weight reduction. It also highlights the importance of this line of gut-brain axis research employing the combined BS and neuroimaging model for identifying longitudinal changes in brain structure that correlated with obesity status.

14 Article Atorvastatin Plus Metformin Confer Additive Benefits on Subjects with Dyslipidemia and Overweight/Obese via Reducing ROCK2 Concentration. 2016

Hao, Z / Liu, Y / Liao, H / Zheng, D / Xiao, C / Li, G. ·The Third People's Hospital of Huizhou, Huizhou, Guangdong Province, China. · The Eastern Hospital of the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong Province, China. ·Exp Clin Endocrinol Diabetes · Pubmed #27123784.

ABSTRACT: BACKGROUND: Atorvastatin and metformin both have pleiotropic effects. Whether atorvastatin combined with metformin could provide additive benefits on subjects with dyslipidemia and overweight/obese is unknown. And the mechanism is also not fully clear yet. METHODS: A cross-sectional research was performed and 130 subjects with dyslipidemia and overweight/obese were enrolled and randomly assigned into combined group (20 mg of atorvastatin daily plus 500 mg of metformin twice daily) and control group (20 mg of atorvastatin daily). At baseline and 8 weeks later, parameters of interest were recorded and fasting venous blood was drawn for laboratory examination. RESULTS: The rates of overweight (76.9% vs. 73.8%) and obese (23.1% vs. 26.2%) in both group were comparable. Dyslipidemia in both groups were featured by increased serum levels of triglyceride (TG), total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C). Serum level of high sensitivity C-reactive protein (Hs-CRP) was comparably elevated in both groups at baseline, and leukocyte rho-associated kinase 2 (ROCK2) and serum nitric oxide (NO) concentrations were also comparable. Generally, the baseline characteristics between these 2 groups were no significant differences. 8 weeks later, compared to baseline, body mass index (BMI), the rates of overweight and obese, daily exercise time, smoking status, lipid profiles, Hs-CRP level, leukocyte ROCK2 and serum NO concentrations in both groups were improved. Notably, compared to control group, the rate of obese, Hs-CRP level, leukocyte ROCK2 and serum NO concentrations were improved more profoundly in the combined group (p<0.05). After adjusted for age, gender, BMI, TG, LDL-C, Hs-CRP and exercise time, atorvastatin plus metformin was positively associated with serum NO concentration, with odds ratio (OR) of 1.146 (95% confidence interval (CI) 1.089-1.164, combined group vs. control group, p<0.05), and inversely associated with leukocyte ROCK2 concentration, with OR of 0.853 (95% CI 0.834-0.872, combined group vs. control group, p<0.05). CONCLUSION: In subjects with dyslipidemia and overweight/obese, atorvastatin plus metformin may confer additive benefits through reducing leukocyte ROCK2 concentration.

15 Article Increased glycogen synthase kinase-3β and hexose-6-phosphate dehydrogenase expression in adipose tissue may contribute to glucocorticoid-induced mouse visceral adiposity. 2016

Yan, C / Yang, H / Wang, Y / Dong, Y / Yu, F / Wu, Y / Wang, W / Adaku, U / Lutfy, K / Friedman, T C / Tian, S / Liu, Y. ·Department of Pediatrics, First Hospital, Jilin University, Chang Chun, People's Republic of China. · Division of Endocrinology, Metabolism and Molecular Medicine, Charles R. Drew University of Medicine and Sciences, UCLA School of Medicine, Los Angeles, CA, USA. · School of Medical Sciences, Hubei University of Chinese Medicine, Wuhan, People's Republic of China. · Vascular Biology Program, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA. · Department of Pharmaceutical Sciences, Western University of Health Sciences, Pomona, CA, USA. · Key Laboratory of Exercise and Health Sciences of Ministry of Education, Shanghai University of Sport, Shanghai, People's Republic of China. ·Int J Obes (Lond) · Pubmed #27102048.

ABSTRACT: BACKGROUND: Increased adiposity in visceral depots is a crucial feature associated with glucocorticoid (GC) excess. The action of GCs in a target tissue is regulated by GC receptor (GR) and 11ß-hydroxysteroid dehydrogenase type 1 (11ß-HSD1) coupled with hexose-6-phosphate dehydrogenase (H6pdh). Glycogen synthase kinase-3β (GSK3β) is known to be a crucial mediator of ligand-dependent gene transcription. We hypothesized that the major effects of corticosteroids on adipose fat accumulation are in part mediated by changes in GSK3β and H6pdh. METHODS: We characterized the alterations of GSK3β and GC metabolic enzymes, and determined the impact of GR antagonist mifepristone on obesity-related genes and the expression of H6pdh and 11ß-HSD1 in adipose tissue of mice exposed to excess GC as well as in in vitro studies using 3T3-L1 adipocytes treated with GCs. RESULTS: Corticosterone (CORT) exposure increased abdominal fat mass and induced expression of lipid synthase acetyl-CoA carboxylase and ATP-citrate lyase with activation of GSK3β phosphorylation in abdominal adipose tissue of C57BL/6J mice. Increased pSer(9) GSK3β was correlated with the induction of H6pdh and 11ß-HSD1. In addition, mifepristone treatment reversed the production of H6pdh and attenuated CORT-mediated production of 11ß-HSD1 and lipogenic gene expression with reduction of pSer(9) GSK3β, thereby leading to improvement of phenotype of adiposity within adipose tissue in mice treated with excess GCs. Suppression of pSer(9) GSK3β by mifepristone was accompanied by activation of pThr(308) Akt and blockade of CORT-induced adipogenic transcriptor C/EBPα and PPARγ. In addition, mifepristone also attenuated CORT-mediated activation of IRE1α/XBP1. In addition, reduction of H6pdh by shRNA showed comparable effects to mifepristone on attenuating CORT-induced expression of GC metabolic enzymes and improved lipid accumulation in vitro in 3T3-L1 adipocytes. CONCLUSION: These findings suggest that elevated adipose GSK3β and H6pdh expression contribute to 11ß-HSD1 mediating hypercortisolism associated with visceral adiposity.

16 Article Association of the FABP2 Ala54Thr polymorphism with type 2 diabetes, obesity, and metabolic syndrome: a population-based case-control study and a systematic meta-analysis. 2015

Liu, Y / Wu, G / Han, L / Zhao, K / Qu, Y / Xu, A / Huang, Q. ·College of Life Sciences, Central China Normal University, Wuhan, China. · Wuhan Center of Medical Therapeutics, Wuhan, China. · Department of Pharmacology and Pharmacy, the University of Hong Kong, Hong Kong, China. · College of Life Sciences, Central China Normal University, Wuhan, China huangqy@mail.ccnu.edu.cn. ·Genet Mol Res · Pubmed #25730055.

ABSTRACT: Previous studies have reported associations between the functional FABP2 Ala54Thr (rs1799883) polymorphism and type 2 diabetes mellitus (T2DM), obesity, and metabolic syndrome in different populations with conflicting results. We investigated the association between the FABP2 Ala54Thr polymorphism and T2DM (235 cases, 431 controls), obesity (377 cases, 431 controls), and metabolic syndrome (315 cases, 323 controls) by logistic regression analysis in a Chinese study cohort recruited from Yichang, Hubei Province. We then comprehensively reviewed the association of the FABP2 Ala54Thr polymorphism with T2DM, obesity, and metabolic syndrome via meta-analysis. The strength of association was assessed by odds ratios (ORs) with 95% confidence intervals (CIs). The FABP2 Ala54Thr polymorphism was significantly associated with obesity (AT vs AA: OR = 2.633, 95%CI = 1.065-6.663, P = 0.036; TT vs AA: OR = 4.160, 95%CI = 1.609-10.757, P = 0.003) and metabolic syndrome (TT vs AA: OR = 2.273, 95%CI = 1.242-4.156, P = 0.008) by logistic regression with adjustment for covariates. However, no significant association was found between T2DM and the FABP2 Ala54Thr polymorphism. We identified 24 studies on T2DM (4517 cases, 5224 controls), 9 studies on obesity (949 cases, 2002 controls), and 6 studies on metabolic syndrome (2194 cases, 3282 controls) by literature search. The meta-analyses revealed significant associations for metabolic syndrome (T allele: OR = 1.179, 95%CI = 1.015-1.362, P = 0.031) and T2DM (T allele: OR = 1.160, 95%CI = 1.08-1.24, P < 0.001), but no association for obesity (T allele: OR = 1.069, 95%CI = 0.925-1.235, P = 0.367).

17 Article Proteomic pattern changes associated with obesity-induced asthenozoospermia. 2015

Liu, Y / Guo, Y / Song, N / Fan, Y / Li, K / Teng, X / Guo, Q / Ding, Z. ·Department of Human Anatomy, Histology and Embryology, Shanghai Key Laboratory for Reproductive Medicine, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. ·Andrology · Pubmed #25293813.

ABSTRACT: Obesity, an increasingly frequent societal disease can also be accompanied by declines in spermatozoa quality and male subfecundity. To determine if there are obesity-associated proteomic changes potentially affecting sperm quality and motility, differential proteomic analysis was performed on spermatozoa from both obesity-associated asthenozoospermia and clinically healthy individuals, using a label-free quantitative LC-MS/MS approach. We resolved 1975 proteins in the human sperm proteome, amongst which, 105 proteins were less abundant, whereas 22 other proteins increased in obesity-associated asthenozoospermia. Functional category analyses indicated that the differentially expressed proteins are mainly related to cytoskeletal regulation, vesicle biogenesis, metabolism, and protein degradation involved in spermiogenesis and sperm motility. Furthermore, declines in endoplasmic reticulum protein 57 (ERp57) and actin-binding-related protein T2 (ACTRT2) expression were verified by immunofluorescence, Western blot, and flow cytometry analyses. It is evident that ERp57 is localized in the acrosome region, neck and principal piece of human spermatozoa, whereas ACTRT2 is localized in the post-acrosomal region and middle piece. Thus, these differences in protein expression in asthenozoospermia may contribute to the underlying sperm quality defects afflicting these individuals. Notably, declines in ERp57 and ACTRT2 expression in obesity-associated asthenozoospermia may play critical roles in reducing sperm motility.

18 Article Candy consumption in childhood is not predictive of weight, adiposity measures or cardiovascular risk factors in young adults: the Bogalusa Heart Study. 2015

O'Neil, C E / Nicklas, T A / Liu, Y / Berenson, G S. ·Louisiana State University Agricultural Center, Baton Rouge, LA, USA. ·J Hum Nutr Diet · Pubmed #24382141.

ABSTRACT: BACKGROUND: There are limited data available on the longitudinal relationship between candy consumption by children on weight and other cardiovascular risk factors (CVRF) in young adults. The present study investigated whether candy consumption in children was predictive of weight and CVRF in young adults. METHODS: A longitudinal sample of children 10 years (n = 355; 61% females; 71% European-Americans, 29% African-Americans) who participated in cross-sectional surveys from 1973 to 1984 (baseline) and in one of two surveys (follow-ups) as young adults [19-38 years; mean (SD) = 23.6 (2.6) years] in Bogalusa, LA, were studied. Dietary data were collected using 24-h dietary recalls at baseline and at one follow-up survey; a food frequency questionnaire was used in the other follow-up survey. Candy consumers were those consuming any amount of candy. Candy consumption was calculated (g day(-1) ) from baseline 24-h dietary recalls, and was used as a covariate in the adjusted linear mixed models. Dependent variables included body mass index (BMI) and CVRF measured in young adults. RESULTS: At baseline, 92% of children reported consuming candy [46 (45) g day(-1)]; the percentage decreased to 67% [20 (30) g day(-1)] at follow-up. No longitudinal relationship was shown between baseline candy consumption and BMI or CVRF in young adults, suggesting that candy consumption was not predictive of health risks later in life. CONCLUSIONS: The consumption of nutrient rich foods consistent with dietary recommendations is important, although modest amounts of candy can be added to the diet without potential adverse long-term consequences to weight or CVRF. Additional studies are needed to confirm these results.

19 Article Dietary intake, plasma homocysteine, and repetitive element DNA methylation in the Multi-Ethnic Study of Atherosclerosis (MESA). 2014

Perng, W / Villamor, E / Shroff, M R / Nettleton, J A / Pilsner, J R / Liu, Y / Diez-Roux, A V. ·Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor, MI, USA. Electronic address: wei.perng@gmail.com. · Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor, MI, USA. · Center for Healthy Communities, Michigan Public Health Institute, Okemos, MI, USA. · Division of Epidemiology, Human Genetics, and Environmental Sciences, University of Texas Health Science Center, Houston, TX, USA. · Department of Environmental Health Science, School of Public Health and Health Sciences, University of Massachusetts, Amherst, MA, USA. · Sticht Center on Aging, Wake Forest University, Winston-Salem, NC, USA. ·Nutr Metab Cardiovasc Dis · Pubmed #24477006.

ABSTRACT: BACKGROUND AND AIMS: DNA methylation of repetitive elements may explain the relations between dietary intake, hyperhomocysteinemia, and cardiovascular disease risk. We investigated associations of methyl micronutrient intake and plasma total homocysteine with LINE-1 and Alu methylation in a cross-sectional study of 987 adults aged 45-84 y who participated in the Multi-Ethnic Study of Atherosclerosis (MESA) Stress Study. METHODS AND RESULTS: DNA methylation was estimated using pyrosequencing technology. A 120-item food frequency questionnaire was used to ascertain daily intake of folate, vitamin B12, vitamin B6, zinc, and methionine. Plasma total homocysteine was quantified using a fluorescence polarization immunoassay. Associations of micronutrient intake and homocysteine with LINE-1 and Alu methylation were examined using linear regression. Adjusted differences in %5-methylated cytosines (%5 mC) were examined by categories of predictors using multivariable linear regression models. Intake of methyl-donor micronutrients was not associated with DNA methylation. After adjustment for covariates, each 3 μmol/L increment of homocysteine corresponded with 0.06 (-0.01, 0.13) %5 mC higher LINE-1 methylation. Additionally, BMI was positively associated with LINE-1 methylation (P trend = 0.03). Participants with BMI ≥ 40 kg/m² had 0.35 (0.03, 0.67) %5 mC higher LINE-1 than those with normal BMI. We also observed a 0.10 (0.02, 0.19) %5 mC difference in Alu methylation per 10 cm of height. These associations did not differ by sex. CONCLUSION: Dietary intake of methyl-donor micronutrients was not associated with measures of DNA methylation in our sample. However, higher BMI was related to higher LINE-1 methylation, and height was positively associated with Alu methylation.

20 Article Ambulatory blood pressure monitoring for risk stratification in obese and non-obese subjects from 10 populations. 2014

Hansen, T W / Thijs, L / Li, Y / Boggia, J / Liu, Y / Asayama, K / Kikuya, M / Björklund-Bodegård, K / Ohkubo, T / Jeppesen, J / Torp-Pedersen, C / Dolan, E / Kuznetsova, T / Stolarz-Skrzypek, K / Tikhonoff, V / Malyutina, S / Casiglia, E / Nikitin, Y / Lind, L / Sandoya, E / Kawecka-Jaszcz, K / Filipovský, J / Imai, Y / Wang, J / O'Brien, E / Staessen, J A. ·Steno Diabetes Centre, Gentofte and Research Centre for Prevention and Health, Glostrup, Denmark. · Studies Coordinating Centre, Division of Hypertension and Cardiovascular Rehabilitation, Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium. · 1] Center for Epidemiological Studies and Clinical Trials, Ruijin Hospital, Shanghai Jiantong University School of Medicine, Shanghai, China [2] Center for Vascular Evaluation, Ruijin Hospital, Shanghai Jiantong University School of Medicine, Shanghai, China. · Centro de Nefrología and Departamento de Fisiopatología, Hospital de Clínicas, Universidad de la República, Montevideo, Uruguay. · 1] Studies Coordinating Centre, Division of Hypertension and Cardiovascular Rehabilitation, Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium [2] Tohoku University Graduate School of Pharmaceutical Science and Medicine, Sendai, Japan. · Tohoku University Graduate School of Pharmaceutical Science and Medicine, Sendai, Japan. · Section of Geriatrics, Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden. · Department of Health Sciences, Shiga University of Medical Sciences, Otsu, Japan. · Copenhagen University Hospital, Copenhagen, Denmark. · Addenbrook's Hospital, Cambridge University Hospitals, Cambridge, UK. · First Department of Cardiology and Hypertension, Jagiellonian University Medical College, Kra-ków, Poland. · Department of Clinical and Experimental Medicine, University of Padova, Padova, Italy. · Institute of Internal Medicine, Novosibirsk, Russian Federation. · The Asociación Española Primera de Socorros Mutuos, Montevideo, Uruguay. · Faculty of Medicine, Charles University, Pilsen, Czech Republic. · Center for Epidemiological Studies and Clinical Trials, Ruijin Hospital, Shanghai Jiantong University School of Medicine, Shanghai, China. · The Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland. · 1] Studies Coordinating Centre, Division of Hypertension and Cardiovascular Rehabilitation, Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium [2] The Department of Epidemiology, Maastricht University, Maastricht, The Netherlands. ·J Hum Hypertens · Pubmed #24430701.

ABSTRACT: Overweight clusters with high blood pressure (BP), but the independent contribution of both risk factors remains insufficiently documented. In a prospective population study involving 8467 participants (mean age 54.6 years; 47.0% women) randomly recruited from 10 populations, we studied the contribution of body mass index (BMI) to risk over and beyond BP, taking advantage of the superiority of ambulatory over conventional BP. Over 10.6 years (median), 1271 participants (15.0%) died and 1092 (12.9%), 637 (7.5%) and 443 (5.2%) experienced a fatal or nonfatal cardiovascular, cardiac or cerebrovascular event. Adjusted for sex and age, low BMI (<20.7 kg m(-2)) predicted death (hazard ratio (HR) vs average risk, 1.52; P<0.0001) and high BMI (> or = 30.9 kg m(-2)) predicted the cardiovascular end point (HR, 1.27; P=0.006). With adjustments including 24-h systolic BP, these HRs were 1.50 (P<0.001) and 0.98 (P=0.91), respectively. Across quartiles of the BMI distribution, 24-h and nighttime systolic BP predicted every end point (1.13 < or = standardized HR < or = 1.67; 0.046 < or = P<0.0001). The interaction between systolic BP and BMI was nonsignificant (P > or = .22). Excluding smokers removed the contribution of BMI categories to the prediction of mortality. In conclusion, BMI only adds to BP in risk stratification for mortality but not for cardiovascular outcomes. Smoking probably explains the association between increased mortality and low BMI.

21 Article Adolescents and young adults with newly diagnosed Type 2 diabetes demonstrate greater carotid intima-media thickness than those with Type 1 diabetes. 2014

Gu, W / Huang, Y / Zhang, Y / Hong, J / Liu, Y / Zhan, W / Ning, G / Wang, W. ·Department of Endocrine and Metabolic diseases, Rui-jin Hospital, Shanghai Jiao-Tong University School of Medicine. ·Diabet Med · Pubmed #24112039.

ABSTRACT: AIM: To compare the carotid intima-media thickness in patients with newly diagnosed Type 1 or Type 2 diabetes ranging from 14 to 30 years of age. METHODS: Demographic, anthropometric and laboratory data were obtained from 404 adolescents and young adults (103 subjects with Type 1 diabetes, 94 with Type 2 diabetes, 153 obese subjects and 54 normal control subjects). Carotid intima-media thickness was assessed based on Doppler ultrasound examination and compared among the four groups. RESULTS: Our data showed significant increases in carotid intima-media thickness in subjects with Type 1 diabetes, Type 2 diabetes and obese subjects compared with the control subjects, with those in the group with Type 2 diabetes demonstrating the greatest change (P < 0.001). Age, BMI, percentage of fat, waist-hip ratio and total triglycerides were significantly correlated with both common and internal carotid intima-media thickness segments. From a stepwise multiple linear regression model, the independent determinants of common carotid intima-media thickness were age, BMI, HbA1c and HDL cholesterol (adjusted R(2)  = 0.152, P < 0.001). After adjustment for age, sex and HbA1c , the odds ratio for increased carotid intima-media thickness was 1.67 (95% CI 1.19-2.33, P = 0.003) for obese subjects, 2.38 (95% CI 1.59-9.47, P = 0.001) for subjects with Type 1 diabetes and 3.93 (95% CI 1.90-6.07, P = 0001) for subjects with Type 2 diabetes compared with the control subjects. CONCLUSIONS: Compared with young control subjects, we found significant increases in carotid intima-media thickness in patients with newly diagnosed Type 1 diabetes and Type 2 diabetes, with patients with Type 2 diabetes showing greater carotid intima-media thickness. Traditional cardiovascular risk factors, such as obesity, dyslipidaemia, hypertension and hyperglycaemia, could cause vessel changes even in adolescents and young adults.

22 Article Short-term aerobic exercise training increases postprandial pancreatic polypeptide but not peptide YY concentrations in obese individuals. 2014

Kanaley, J A / Heden, T D / Liu, Y / Whaley-Connell, A T / Chockalingam, A / Dellsperger, K C / Fairchild, T J. ·Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO, USA. · Department of Internal Medicine, Division of Nephrology Internal Medicine, Columbia, MO, USA. · Department of Internal Medicine, Division of Cardiovascular Medicine, Columbia, MO, USA. · 1] Department of Internal Medicine, Division of Nephrology Internal Medicine, Columbia, MO, USA [2] Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO, USA. · School of Chiropractic and Sports Science, Murdoch University, Murdoch, Western Australia, Australia. ·Int J Obes (Lond) · Pubmed #23736355.

ABSTRACT: OBJECTIVE: Short-term exercise training improves glycemic control, but the effect of short-term training on postprandial satiety peptide responses or perceived satiety remains unknown. We tested the hypothesis that short-term aerobic exercise training (15 days) would alter postprandial pancreatic and gut peptide (pancreatic polypeptide (PP) and peptide YY (PYY)) responses and perceived appetite and satiety in obese individuals. SUBJECTS: Thirteen healthy obese men and women (age: 42±2 years; body mass index: 30-45 kg m(-2)). MEASUREMENTS: Subjects were studied before and after 15 days of training (walking 1 h at 70-75% VO(2peak)). On the study day, subjects consumed 1500 kcal as six meals (250 kcal: 9 g protein, 40 g carbohydrate, 6 g fat), while blood samples and satiety measurements were taken at baseline and every 20 min for 12 h. Blood was analyzed for PP, PYY, glucose and insulin levels. Appetite and satiety was assessed with a visual analog scale throughout the day. RESULTS: Incremental area under the curve (iAUC) for PP increased significantly with training (pre: 2788±753; post: 3845±830 pg ml(-1)·per min for 12 h; P<0.001), but there was no difference in the PP response to each meal. The initial PP response to the first meal increased (ΔPP(min 20-0): pre 86±25; post 140±36 pg ml(-1); P<0.05) with training. PYY iAUC showed no significant changes with training but showed a significant main effect of time across meals, with the largest response being to the first meal (P<0.005). There were no changes in satiety, glucose or insulin levels with training. CONCLUSION: Short-term exercise training increases postprandial PP concentrations in obese individuals; however, PYY levels and glycemic control remain unaffected. Both PP and PYY show meal-induced increases at all meals, but PYY has a greater response at the first meal with reduced responses at subsequent meals.

23 Article Lipoprotein receptor-related protein 1 variants and dietary fatty acids: meta-analysis of European origin and African American studies. 2013

Smith, C E / Ngwa, J / Tanaka, T / Qi, Q / Wojczynski, M K / Lemaitre, R N / Anderson, J S / Manichaikul, A / Mikkilä, V / van Rooij, F J A / Ye, Z / Bandinelli, S / Frazier-Wood, A C / Houston, D K / Hu, F / Langenberg, C / McKeown, N M / Mozaffarian, D / North, K E / Viikari, J / Zillikens, M C / Djoussé, L / Hofman, A / Kähönen, M / Kabagambe, E K / Loos, R J F / Saylor, G B / Forouhi, N G / Liu, Y / Mukamal, K J / Chen, Y-D I / Tsai, M Y / Uitterlinden, A G / Raitakari, O / van Duijn, C M / Arnett, D K / Borecki, I B / Cupples, L A / Ferrucci, L / Kritchevsky, S B / Lehtimäki, T / Qi, Lu / Rotter, J I / Siscovick, D S / Wareham, N J / Witteman, J C M / Ordovás, J M / Nettleton, J A. ·Nutrition and Genomics Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA, USA. ·Int J Obes (Lond) · Pubmed #23357958.

ABSTRACT: OBJECTIVE: Low-density lipoprotein-related receptor protein 1 (LRP1) is a multi-functional endocytic receptor and signaling molecule that is expressed in adipose and the hypothalamus. Evidence for a role of LRP1 in adiposity is accumulating from animal and in vitro models, but data from human studies are limited. The study objectives were to evaluate (i) relationships between LRP1 genotype and anthropometric traits, and (ii) whether these relationships were modified by dietary fatty acids. DESIGN AND METHODS: We conducted race/ethnic-specific meta-analyses using data from 14 studies of US and European whites and 4 of African Americans to evaluate associations of dietary fatty acids and LRP1 genotypes with body mass index (BMI), waist circumference and hip circumference, as well as interactions between dietary fatty acids and LRP1 genotypes. Seven single-nucleotide polymorphisms (SNPs) of LRP1 were evaluated in whites (N up to 42 000) and twelve SNPs in African Americans (N up to 5800). RESULTS: After adjustment for age, sex and population substructure if relevant, for each one unit greater intake of percentage of energy from saturated fat (SFA), BMI was 0.104 kg m(-2) greater, waist was 0.305 cm larger and hip was 0.168 cm larger (all P<0.0001). Other fatty acids were not associated with outcomes. The association of SFA with outcomes varied by genotype at rs2306692 (genotyped in four studies of whites), where the magnitude of the association of SFA intake with each outcome was greater per additional copy of the T allele: 0.107 kg m(-2) greater for BMI (interaction P=0.0001), 0.267 cm for waist (interaction P=0.001) and 0.21 cm for hip (interaction P=0.001). No other significant interactions were observed. CONCLUSION: Dietary SFA and LRP1 genotype may interactively influence anthropometric traits. Further exploration of this, and other diet x genotype interactions, may improve understanding of interindividual variability in the relationships of dietary factors with anthropometric traits.

24 Minor Effects of a very low-calorie diet on insulin sensitivity and insulin secretion in overweight/obese and lean type 2 diabetes patients. 2015

Liu, C / Li, C / Chen, J / Liu, Y / Cheng, Q / Xiang, X / Chen, G. ·Endocrine and Diabetes Center, Jiangsu Province Hospital on Integration of Chinese and Western Medicine, Nanjing University of Traditional Chinese Medicine, Jiangsu Branch of China Academy of Chinese Medical Science, Nanjing, People's Republic of China. · Nutrition Department, Jiangsu Province Hospital on Integration of Chinese and Western Medicine, Nanjing University of Traditional Chinese Medicine, Jiangsu Branch of China Academy of Chinese Medical Science, Nanjing, People's Republic of China. · Endocrine and Diabetes Center, Jiangsu Province Hospital on Integration of Chinese and Western Medicine, Nanjing University of Traditional Chinese Medicine, Jiangsu Branch of China Academy of Chinese Medical Science, Nanjing, People's Republic of China. Electronic address: guofangchen@hotmail.com. ·Diabetes Metab · Pubmed #26439662.

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